By Icon Health Publications
It is a 3-in-1 reference booklet. It offers a whole scientific dictionary masking 1000s of phrases and expressions in terms of cardiomyopathy. It additionally offers wide lists of bibliographic citations. eventually, it offers info to clients on find out how to replace their wisdom utilizing quite a few web assets. The booklet is designed for physicians, clinical scholars getting ready for Board examinations, scientific researchers, and sufferers who are looking to familiarize yourself with examine devoted to cardiomyopathy. in case your time is effective, this e-book is for you. First, you won't waste time looking out the net whereas lacking loads of appropriate info. moment, the booklet additionally saves you time indexing and defining entries. eventually, you won't waste money and time printing 1000's of web content.
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Extra resources for Cardiomyopathy - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
To elucidate signaling mechanisms, we will determine which of the major Gi pathways in the heart (Gi2 and Gi3) are involved; and whether signaling via the G protein alpha subunit and/or the betagamma dimer is involved. Using 3 model systems we will investigate Gi signaling effects (both deleterious and beneficial) and the ec-couplingand signaling mechanisms involved in: Aim 1. CHF caused by Ro1 expression; and recovery after terminating Ro1 expression. Aim 2. Acute Cardioprotection caused by Ro1 expression.
Professor; Medicine; Indiana UnivPurdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 01-JAN-1999; Project End 31-DEC-2003 Summary: Clinical recovery from myocardial infarction is thwarted, in part, by inability of surviving ventricular myocytes to reconstitute functional cardiac mass through a corresponding, compensatory increase in cell number. This highlights the limited capacity to restore cardiac mass by hypertrophy alone, and deleterious effects associated with hypertrophy that further impair survival.
In addition, this Core will also characterize the in vivo ventricular performance of the hearts within the transgenic mice. The long-term goals are: 1) to utilize FHCrelated point mutations as a means of identifying key structural domains within the mutant sarcomeric proteins and to determine how these domains relate to the protein's molecular function; 2) to understand how point mutations in contractile proteins compromise sarcomere function, and how these mutations, in turn, may trigger cardiac hypertrophy.